Circ-NFKB1 sponges miR-203a-5p to regulate ERBB4 expression and promotes IL-1β induced chondrocytes apoptosis
Abstract Background Osteoarthritis (OA) is a chronic disease of the bones and joints that commonly affects middle-aged and elderly individuals, characterized by the degeneration of articular cartilage and inflammation of the joints. The molecular mechanisms of OA urgently need to be further examined...
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| Format: | Article |
| Language: | English |
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BMC
2023-07-01
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| Series: | Journal of Orthopaedic Surgery and Research |
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| Online Access: | https://doi.org/10.1186/s13018-023-03990-4 |
| _version_ | 1797769379203514368 |
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| author | Zhao Wang Hongwei Bao Jingzhao Hou Bin Ju Yong Ji |
| author_facet | Zhao Wang Hongwei Bao Jingzhao Hou Bin Ju Yong Ji |
| author_sort | Zhao Wang |
| collection | DOAJ |
| description | Abstract Background Osteoarthritis (OA) is a chronic disease of the bones and joints that commonly affects middle-aged and elderly individuals, characterized by the degeneration of articular cartilage and inflammation of the joints. The molecular mechanisms of OA urgently need to be further examined. Our study intended to uncover circ-NFKB1/miR-203a-5p/ERBB4 axis in regulating interleukin-1β (IL-1β) induced chondrocytes apoptosis. Methods GSE178724, GSE79258 and GSE169077 were downloaded from Gene Expression Omibus (GEO) database and differentially expressed circRNAs, miRNAs and mRNAs were obtained by R software. Annexin V assay was used to determine cell apoptosis rate. ELISA was further performed to identify the inflammation response. Dual-luciferase reporter gene assay was conducted to examine the combination among circ-NFKB1, miR-203a-5p and ERBB4. Results Our research demonstrated that circ-NFKB1 and ERBB4 were significantly upregulated through bioinformatic analysis. MiR-203a-5p was significantly downregulated through bioinformatic analysis. Silencing of circ-NFKB1 notably inhibited the IL-1β induced chondrocytes apoptosis and upregulated ERBB4 expression. Through prediction on bioinformatics analysis, miR-203a-5p was the target binding circ-NFKB1, and ERBB4 was the potential target of miR-203a-5p. Subsequently, these changes induced by the silencing of circ-NFKB1 were reversed upon addition of pcDNA/ERBB4. Conclusions Silencing circ-NFKB1 could sponge miR-203a-5p to regulate ERBB4 expression and alleviate OA progression. |
| first_indexed | 2024-03-12T21:08:14Z |
| format | Article |
| id | doaj.art-99dd01797ee14df099e9c47d5a4254ba |
| institution | Directory Open Access Journal |
| issn | 1749-799X |
| language | English |
| last_indexed | 2024-03-12T21:08:14Z |
| publishDate | 2023-07-01 |
| publisher | BMC |
| record_format | Article |
| series | Journal of Orthopaedic Surgery and Research |
| spelling | doaj.art-99dd01797ee14df099e9c47d5a4254ba2023-07-30T11:20:46ZengBMCJournal of Orthopaedic Surgery and Research1749-799X2023-07-0118111410.1186/s13018-023-03990-4Circ-NFKB1 sponges miR-203a-5p to regulate ERBB4 expression and promotes IL-1β induced chondrocytes apoptosisZhao Wang0Hongwei Bao1Jingzhao Hou2Bin Ju3Yong Ji4Department of Orthopedics, Jingjiang People’s HospitalDepartment of Orthopedics, Jingjiang People’s HospitalDepartment of Orthopedics, Jingjiang People’s HospitalDepartment of Medical Imaging, Jingjiang People’s HospitalDepartment of General Surgery, Jingjiang People’s HospitalAbstract Background Osteoarthritis (OA) is a chronic disease of the bones and joints that commonly affects middle-aged and elderly individuals, characterized by the degeneration of articular cartilage and inflammation of the joints. The molecular mechanisms of OA urgently need to be further examined. Our study intended to uncover circ-NFKB1/miR-203a-5p/ERBB4 axis in regulating interleukin-1β (IL-1β) induced chondrocytes apoptosis. Methods GSE178724, GSE79258 and GSE169077 were downloaded from Gene Expression Omibus (GEO) database and differentially expressed circRNAs, miRNAs and mRNAs were obtained by R software. Annexin V assay was used to determine cell apoptosis rate. ELISA was further performed to identify the inflammation response. Dual-luciferase reporter gene assay was conducted to examine the combination among circ-NFKB1, miR-203a-5p and ERBB4. Results Our research demonstrated that circ-NFKB1 and ERBB4 were significantly upregulated through bioinformatic analysis. MiR-203a-5p was significantly downregulated through bioinformatic analysis. Silencing of circ-NFKB1 notably inhibited the IL-1β induced chondrocytes apoptosis and upregulated ERBB4 expression. Through prediction on bioinformatics analysis, miR-203a-5p was the target binding circ-NFKB1, and ERBB4 was the potential target of miR-203a-5p. Subsequently, these changes induced by the silencing of circ-NFKB1 were reversed upon addition of pcDNA/ERBB4. Conclusions Silencing circ-NFKB1 could sponge miR-203a-5p to regulate ERBB4 expression and alleviate OA progression.https://doi.org/10.1186/s13018-023-03990-4Circ-NFKB1miR-203a-5pERBB4OsteoarthritisApoptosis |
| spellingShingle | Zhao Wang Hongwei Bao Jingzhao Hou Bin Ju Yong Ji Circ-NFKB1 sponges miR-203a-5p to regulate ERBB4 expression and promotes IL-1β induced chondrocytes apoptosis Journal of Orthopaedic Surgery and Research Circ-NFKB1 miR-203a-5p ERBB4 Osteoarthritis Apoptosis |
| title | Circ-NFKB1 sponges miR-203a-5p to regulate ERBB4 expression and promotes IL-1β induced chondrocytes apoptosis |
| title_full | Circ-NFKB1 sponges miR-203a-5p to regulate ERBB4 expression and promotes IL-1β induced chondrocytes apoptosis |
| title_fullStr | Circ-NFKB1 sponges miR-203a-5p to regulate ERBB4 expression and promotes IL-1β induced chondrocytes apoptosis |
| title_full_unstemmed | Circ-NFKB1 sponges miR-203a-5p to regulate ERBB4 expression and promotes IL-1β induced chondrocytes apoptosis |
| title_short | Circ-NFKB1 sponges miR-203a-5p to regulate ERBB4 expression and promotes IL-1β induced chondrocytes apoptosis |
| title_sort | circ nfkb1 sponges mir 203a 5p to regulate erbb4 expression and promotes il 1β induced chondrocytes apoptosis |
| topic | Circ-NFKB1 miR-203a-5p ERBB4 Osteoarthritis Apoptosis |
| url | https://doi.org/10.1186/s13018-023-03990-4 |
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